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Cancer

Prevention is MUCH better than cure

The cancer institutions’ annual reports are glossy affairs, full of positive news items about increased survival times and yet more ‘breakthrough’ drugs. I support their work and there is good news. But behind the scenes, the scientists are not quite so optimistic. After all we in the West have a 1 in 2 chance of contracting cancer at some point in our lives.

In an influential review in the New England Journal of Medicine (Bailar & Gornik ’97), the authors concluded:

‘The war against cancer is far from over. Observed changes in mortality due to cancer primarily reflect changing incidence or early detection. The effect of new treatments for cancer on mortality has been largely disappointing. The most promising approach to the control of cancer is a national commitment to prevention, with a concomitant rebalancing of the focus and funding of research.’

There are more positive voices in cancer research, and there are undoubtedly interesting and important developments in the pipeline; but the shift in emphasis called for in the review (above) has still not occurred. Profit is what appears to drive much of the world, and there is no great profit to be made in cancer prevention. The drug companies still make their money from magic bullets designed to kill cancer cells; but in the area of cancer, where the enemy cells are so very like the host, the risks of collateral damage are very high indeed.

During the ’70s and ’80s a drug company had to submit two favourable, large randomised trials to obtain US Food and Drug Administration (FDA) approval for a new drug. “Favourable” meant that there must be a certain rate of tumour shrinkage lasting for at least one month. It was not necessary to show that the treatment prolonged survival, and it was not necessary to submit the results of any unfavourable results from the same drug.

These guidelines, already less than stringent, were relaxed further in the ’90s. Drug companies can now get FDA approval on the basis of small preliminary trials, even if a large randomised trial may subsequently give unfavourable results. In a remarkable statement about drug approvals, an FDA spokesperson pointed out that any delay in approval did not mean unnecessary deaths because “none of the treatments for advanced cancer cure people”.

The truth is that cancer is at an all-time high. It is also very likely that in the near future we will see cancer figures rising yet further, fuelled in part by the staggering increases in overweight and obesity that are occurring all over the world. Because as we get fatter, we become more likely to develop a range of cancers (Bianchini et al ’02, Calle et al ’03, Freedland et al ’05).

The huge research effort into cancer has produced treatments which are less than rigorously screened, are non-curative, which may extend life in some cases – but are generally toxic, responsible for many adverse effects, are powerful carcinogens in their own right (Klein–Szanto ’92), and too often ineffective or even counter-productive (Chute et al ’97, Lassen et al ’98, PORT ’98, Rougier et al ’98, Bandealy et al ’98, Wolmark et al 2000, Riccardi et al 2000, Schulman et al ’03).

If this strikes you as a poor bargain, many cancer specialists would agree. 18 years ago, when 118 oncologists at a major cancer institute in the United States were asked whether they would opt for chemotherapy if they were diagnosed with non-small-cell lung cancer, three-quarters said they would turn down the treatment.

Why? “Ineffective and unacceptably poisonous.” (Mackillop et al ’87)

The cancer concerned was (and is) a difficult one to treat – but hardly unique in that respect. And although the question has not been formally asked since, my own experience with oncologists leads me to believe that the majority of them would still not willingly accept chemotherapy for many cancers.

However, I do not want to be too pessimistic – it IS true that survival rates of people living with cancer are increasing. And the fact that death rates have not leapt up in parallel with incidence rates is testimony to the fact that there have been improvements in palliative therapy. However, the fact that the incidence rates have also risen so far in so short a period of time (effectively, within two generations) shows that we have failed to make any progress in terms of disease prevention.

But let’s start by looking at a significant success.

Better screening, earlier detection

There is a strong case for better screening and earlier detection of cancer; earlier detection means, usually, a better prognosis. The best-known screening programmes are for cervical, breast, bowel and prostate cancer; but though these programmes have undoubted benefits, they carry costs and risks of their own.

Cervical cancer
The oldest, most successful, and most cost-effective of all the screening programmes, in the UK cervical screening led to a fall in cervical cancer of 42 per cent between 1988 and 1997 (Nat Stat 2000). This type of screening is therefore highly effective.

Breast cancer
The NHS Breast Screening Programme provides free screening for all women over the age of 50, and is considered to be an outstanding example of its kind. The programme has screened more than 14 million women and detected over 80,000 cancers since it went nationwide in the mid-’90s.

This level of screening (and investment) has reduced death rates from breast cancer in women aged 55-69 and by the late ’90s was, according to one research paper, saving over 300 lives per year (Blanks et al 2000).

Bowel cancer
In two large trials, physical screening of 100,000 individuals (using colonoscopy) resulted in the early detection of bowel cancer in 35 people, who, as a consequence, had their life expectancy prolonged.

Another method of screening is the Faecal Occult Blood (FOB) test, which detects non-visible blood in the stool. It is non-invasive and relatively inexpensive, but is considerably less accurate than colonoscopy. Nevertheless, routine screening of people over the age of 50 reduces the mortality rate for bowel cancer (Hardcastle et al ’96), and the UK National Bowel Cancer Screening Programme, initially scheduled to start in April 2006, was projected to save about 1200 lives per year (Atkin ’99).

Prostate cancer
The main problem with routine prostate cancer screening is that even though this malignancy is extremely common, occurring in about 70 percent of 80-year-olds (Pienta ’97), it is the cause of death in only 3% of men (Silverberg & Lubera ’86). In other words, most prostate cancers grow so slowly that no symptoms ever appear, because most patients die of other causes before the prostate cancer can cause any serious problem.

This means that prostate cancer screening programs detect many ‘silent’ cancers that will have no impact on the patient’s life expectancy. This creates problems both for the patient and the doctor because, while many cancers do not affect the patient’s quality of life, many of the treatments undoubtedly do.

From a medical point of view it is entirely reasonable to screen for prostate cancer when there are other symptoms present. However, by that stage the cancer is generally quite advanced and the prognosis poor whether treatment is offered or not.

Cancer screening – the verdict

The huge investment in cancer screening programmes has undoubtedly saved and will continue to save lives. But here again, as with the even more massive investment in cancer treatment, we are attempting to lock the stable door after the horse has bolted. A little faster off the mark, perhaps, but still late in the day. And once a cancer has been detected, the treatments still rely on surgery, chemo- and radio-therapy.

Given that cervical, breast, bowel and prostate cancers (and other cancers such as melanoma) have all doubled in the last 55 years, I would submit that our anti-cancer strategies appear to be fundamentally out of proportion.

1. Despite knowing that as many as 40% of cancers are due to life-style factors and are therefore avoidable, research into effective cancer prevention programmes is starved of funds.

2. Despite knowing a great deal about the way in which dietary factors can modify cancer cells, nutritional cancer management programmes are similarly starved.

3. And despite the overwhelming evidence that dietary changes are, along with smoking cessation, the most powerful way of reducing risk, health education spending is pitifully small when compared with drug industry funding.

Prevention is better than cure is perhaps more true of cancer than for any other disease.

Better Prevention: Diet & Nutrition

The most widely recognised way to reduce risk of cancer is by making lifestyle and dietary changes.

– Giving up smoking is the single most effective step you can take – if you are a smoker.
– Weight loss, where appropriate, and increased levels of physical exercise, are next in line.
– By dietary change, most authorities mean giving more emphasis to plant foods and eating less meat.

This UK-based organization recommends five or more portions of vegetables and fruit daily, and “if eaten at all, red meat to provide no more than 10% of total calories”. They claim that “30 to 40 per cent of cancer cases could be prevented by making healthier food and lifestyle choices”.

A more specific clinical review (Cummings & Bingham ’98) concluded: “Up to 80% of bowel and breast cancer may be preventable by dietary change. Diet contributes to varying extent to the risk of many other cancers, including cancers of the lung, prostate, stomach, oesophagus, and pancreas… Generally, fruit, vegetables, and fibre have a protective effect, whereas red and processed meat, increase the risk of developing cancer.”

Conversely there is a clear correlation between meat intake and cancer. Those countries that have the highest intakes of meat (eg Denmark, UK, Canada, US) have the highest incidents of cancer. Those countries with the lowest intakes of meat (eg Japan, Hong Kong, Chile, Portugal) have the lowest incidents of cancer.

But How Much?

Although plant foods are generally agreed to be protective, there is substantial disagreement as to how much fruit and vegetables we need to eat.

The World Cancer Research Fund, the World Health Organisation, the Europe Against Cancer organisation, the US National Cancer Institute and our very own Department of Health all support the five-a-day strategy. However, they were taken aback by a recent and extensive study (Hung et al ’04) which indicated that around 5 portions of fruit and vegetables a day slightly reduced the risk of heart disease, but this level of intake had little effect on cancer.

The US-based National Cancer Institute (NCI) goes further, and recommends that women should eat 7 portions of fruit and vegetables a day; men are instructed to eat 9 portions a day. For more information, go to: http://www.5adaygov/9aday/).

At Tufts University, Professor Jim Joseph and his team, who specialise in studying the impact of plant foods on human biochemistry, have come out with a recommended ‘dose’ of around 10 portions of fruit and vegetables per day. Some in his department have said, off the record, that optimal levels of intake might be even higher!

In 2005 the US Agriculture Department and the Department of Health and Human Services jointly issued new guidelines recommending that in addition to the daily intake of fruits and veg every adult should eat:

3 portions of whole-grain foods per day;
And per week:
At least three portions of dark-green vegetables such as broccoli or spinach
Two portions of orange vegetables such as carrots and squash
Three portions of legumes such as lentils and chickpeas
Six portions of starchy vegetables such as potatoes, corn and green peas
Seven portions of other vegetables such as tomatoes, onions and lettuce.

Phew!

Given that we are being bombarded with the 5-a-day dietary guidelines, how do we confused consumers actually manage?

The answer is, not very well … In the US, public awareness has risen to the point where average intakes of fruit and veg are now hovering around the 3 mark. The English clock in at around 2.5 portions, and the Scots come an unhealthy last with less than 1 portion a day!! It is no coincidence that the Scots top the international league tables for heart attacks, and fare poorly in the cancer statistics too.

Why, despite general agreement that fruit and vegetables are good for you, do people persist in eating diets that condemn them to premature ill health and death? Consumers typically respond that fruit and veg can be expensive and inconvenient; that it is physically difficult (if not impossible) to eat 9 portions a day; that you can’t get children to eat the stuff; and that anything not eaten rapidly ‘goes off’ so that too much is wasted.

Apart from boosting your fruit and vegetable intake, what more can we do to cut the risk of cancer?

Cancer Prevention – The Pharmaco-Nutritional Strategy

Let’s abandon, for the moment, the old-fashioned idea of regarding the cancer cell as an enemy to be shot on sight. This historic approach has really been a monumental failure; it is expensive, non-curative and highly toxic. Let us instead reverse the perspective, and look instead at the life and hard times of the ‘poor little cancer cell’.

We think of cancer as a single disease: a single accident produces a rogue cell that multiplies over time, growing into a tumour which eventually becomes large enough to cause symptoms.

Nothing could be further from the truth. A typical human body contains about 5 x 1013 cells. (Many trillions.)

Hundreds of these cells turn cancerous every day, because our cells are bathed in a carcinogenic environment containing radiation-related, environmental, dietary and pathogenic carcinogens. So the real question is, why do so few cancers develop?

The answer is that we have very well organised and multiple defences against cancer – about 10 different defence systems at the last count; and when these defences are working properly, the vast majority of cancerous cells (perhaps 99.99999%) are neutralised before they can cause any problems.

Only an estimated 1 cancer cell in 4 million manages to overcome all of our many defences and grow successfully into a clinically significant entity IF your many defence systems are working well. But if your defences are impaired, the odds may shorten to 1 in a million – a four-fold increase in your cancer risk, equating to a 1 in 2 life-time risk.

The global statistics (Fig 1) hint that in some parts of the world, lifestyle and particularly dietary factors make for strong defences; while in other regions the defences are impaired. So some of my recommendations flow from analysing the low cancer area diets.

To begin with, it is actually very difficult for a cell to become cancerous. As each cell contains many ‘on’ and ‘off’ switches, a single mutation is rarely sufficient to persuade a normal cell to ‘jump the tracks’. It is estimated that between 6 and 8 genetic mutations must take place in order for a normal cell to become a cancer cell.

There’s a balancing act going on here: on the one hand, the DNA in each of our cells gets around 100 ‘hits’ a day from background radiation (Shigenaga et al ’89, Fraga et al ’91); but on the other, our cells contain highly efficient DNA repair mechanisms which patrol the DNA looking for errors and repairing them.

The DNA repair system is very robust, but nonetheless cancerous sells are continuously appearing. This may sound alarming but is not an immediate problem because the vast majority of cancer cells die very quickly, due to oxidative stress and/or the immune system, which identifies the cells as abnormal and kills them off. (See section on Immune Threats ). Those cancer cells which manage to avoid these two defences, still have a long way to go …
OUR MULTIPLE ANTI-CANCER DEFENCES

Let’s first list the defence mechanisms – and then explain them, so don’t worry about the terminology!

1. Excessive levels of free radicals
Excessive free radicals cause DNA damage. Potentially dangerous free radicals are mopped up in the body by antioxidant enzymes (such as glutathione peroxidase, superoxide dismutase etc), and by antioxidant compounds such as vitamins C and E, phytonutrients such as lycopene and the flavonoids, various proteins and steroids, and many others.

The antioxidant enzymes all require mineral co-factors such as selenium, iron, copper, zinc and manganese. The characteristic Western diet is depleted in all of these (Type B malnutrition), and is low also in the antioxidants and phyto-nutrients. In many people, therefore, this first line of defence is not working as effectively as it should.

2. Detoxification
Potentially carcinogenic compounds in our food and environment can cause DNA mutations. Our second line of defence consists of two groups of enzymes called Phase 1 and Phase 2 enzymes. Phase 2 enzymes are the more broadly effective; their main role is to make carcinogens more easily excreted from the body.

The Phase 2 enzymes are activated by various foods such as broccoli, cabbage and Brussels sprouts which contain cancer-fighting phytonutrients like indoles, carbinols and glucosinolates (Fahey & Talalay ’99, Brooks et al ’01).

The typical Western diet is historically inadequate in all these protective elements; so the second line of defence is working at less than capacity also.

3. Suppression of oncogenes
There are certain genes in our DNA (called oncogenes) which switch cancers on. If these genes are methylated (chemically altered) they become less active (Herbert ’01, Herbert ’02). The methylation reaction depends on adequate dietary intake of methyl group nutrients such as the B vitamin family – B6, B12, folic acid and betaine.

The Western diet is low in all these nutrients, as shown by the prevalence of excess homocysteine – an unhealthy shift in blood chemistry which occurs when there are insufficient of B family vitamins in the diet – and so this line of defence is down too. B vitamins are found in whole grains, fish, eggs, kidney and liver, and meat.

4. Colonic microflora
A healthy population of bacteria in the gut is a powerful anti-cancer defence system; and by eating the right diet (ie one which contains significant levels of pre-biotic fibre), the healthy bacteria are encouraged to grow and protect us. Pre-biotic fibre is found in legumes, lentils, beans, and chicory, and is commercially available as an extract from corn or wheat.

Western consumers are historically low in all these elements. Beta sitosterol consumption has fallen because of decreased intakes of seeds, nuts and whole grains. Vitamin D levels have fallen due to decreased levels of foods such as sardines and dairy in our diet, and our modern phobias about sun exposure.

Amounts of 1-3, 1-6 beta glucans in our diet have fallen due to improved standards of food storage and hygiene. This has ensured that levels of yeasts and other micro-organisms, which contain beta glucans in their cell walls, are far below those we used to encounter before canning and freezing technology became universal. This line of defence therefore is impaired also.

5. B) The acquired (specific) immune system
This is a more recently evolved part of the immune system, which has ‘memory’ and is able to mount very specific antibody defences. This system requires adequate calories and protein, but also arginine, omega 3 fatty acids and many different micronutrients like the minerals copper and zinc, the vitamins C and E, and key phytonutrients such as beta carotene in order to function at peak effectiveness (Daly et al ’92, Kemen et al ’95, Schilling et al ’96, Heys et al ‘99).
The Western diet has become low in all these elements; so that the acquired immune defence is, like all the others, out of kilter.

6. Cell contact inhibition
When normal cells come into contact with each other they stop growing. This phenomenon is called ‘cell contact inhibition’. It is mediated by molecules on the cells’ membranes called connexins, the most prevalent of which is Connexin 43, or C43.

Cancer cells generally have lower levels of connexins on their membranes, and therefore when they come into contact with other cells they do not stop growing. Some nutritional elements, however, can force cancer cells to re-grow their connexins; and when they do, they become subject once more to the normal constraints to growth. The carotenoids ( eg beta carotene, alpha carotene, lycopene and lutein) are particularly effective in forcing cancer cells to re-grow connexins (Bertram ’99).

Sadly, levels of carotenoids in the Western diet have fallen to an all-time low; and so this line of anti-cancer defence is down also.

7. Re-differentiation / apoptosis inducers
When a cell turns cancerous, it de-differentiates; that is it becomes amorphous and gradually loses the characteristic features of the cells in the tissue from which it originally came. There are a number of elements in our diet that have the ability to force cancer cells to either commit suicide, (called apoptosis), or re-differentiate, in which case they become once more like their original selves.

When this happens, they become more normal and significantly less cancerous. Dietary elements which have the ability to do this include carotenoids and xanthophylls such as alpha-carotene, lycopene and astaxanthin (Sharoni et al ’02); isoflavones from soy such as genistein, daidzein and glycetin (Constantinou & Huberman ’95); butyrate (formed in the presence of pre-biotics) (Heerdt et al ’94), and the vitamins D (Amir et al ’99) and A (Hansen et al ’04).

8. Cell cycle arrest / apoptosis inducers
These compounds overlap with the previous line of defence, but differ slightly in that, as well as inducing apoptosis (ie cell death), they can also stop cancer cells from dividing.

The Western diet is low in all of these, so yet another anti-cancer defence is sub-optimally effective.

9. Physical barriers to growth: 1
The Extra-Cellular Matrix (ECM) is a fine mesh of micro-fibres which holds all of our cells in place. If angiogenesis (which is the growth of new blood vessels to fuel tumour growth) and metastatic spread are to occur, the ECM must first be breached.

The integrity of the ECM is therefore highly important; and as it is constantly being broken down, it must also constantly be repaired. This requires a variety of micronutrients including vitamins C and B6; the trace elements zinc, copper and manganese; and various amino sugars including glucosamine.

In many cases the Western diet is too low in all of these, leading to accelerated age-related degeneration of the matrix and the degradation of another layer of anti-cancer defence.

10. Physical barriers to growth: 2
As we have seen, successful cancer cells break down the ECM by secreting two different kinds of enzymes called Proteases and Matrix Metallo-Proteases (or MMPs), of which there are over 17 identified so far.

The more MMPs a cancer produces, the more malignant it is (Zucker et al ’99), and the worse the prognosis (Murray et al ’96, Murray et al ’98).

There are various compounds in foods which block the Proteases called Protease Inhibitors, such as the Birk-Bowman Protease Inhibitor in soy (Witschi & Kennedy ’89, Meyskens ’01), and other compounds that block MMPs, called MMP-inhibitors, such as the oligomeric proanthocyanidins found in berry fruits.

The Western diet is historically low in all these elements; so that the cancer cells’ chances of overcoming this last barrier are increased also.

SUMMARY

Cells in our bodies are constantly becoming cancerous. The chances of these cancer cells surviving ‘successfully’ depend on their ability to overcome our multiple lines of anti-cancer defence. The way we live and eat has left all of these defence lines below par. This has made a very significant contribution to the historically high levels of cancer we see today.

If we changed our diets in a way that would provide our multiple defence systems with all the micro- and phyto-nutrients they need to operate as they should, far more cancerous cells would be killed off before they could become clinically overt, and we would really start to win the war against cancer.

Just a theory? Not quite … in an important recent paper, Professor Dean Ornish and his research team at the University of California looked at the impact of diet in 93 men with early prostate cancer (Ornish et al ’05). Half the patients were given a vegan diet of fruits, vegetables, whole grains, beans, and soy products instead of dairy . The other half continued to eat their normal diet; and the experiment ran for a period of 12 months.

In the latter group, and very much as expected, 6 patients (ie 1 in 7) were forced by the year’s end to receive conventional anti-cancer therapy because their PSA scores had risen significantly and their cancers had grown.

In dramatic contrast, not one single patient in the experimental group showed sufficient deterioration to warrant conventional treatment. Their cancers had not grown, and their PSA scores had actually fallen.

An additional finding which helped to explain these amazing benefits was that serum from the experimental group contained sufficient levels of anti-cancer micro-nutrients to inhibit the growth of prostate cancer cells 8 times more effectively than serum from the normal diet group.

This was a critically important piece of research, but it is only a first step. The experimental diet in this paper was not specifically designed to protect against cancer, and was in fact originally intended to reduce the risk of heart disease. If we start from an analysis of all the known anti-cancer micro- and phyto-nutrients, we can assemble a far more comprehensive cancer protection program.

An ideal diet would bathe our cells in a sea of all these anti-cancer nutrients, shore up all of our anti-cancer defences; and would be expected to be even more protective than the diet in the University of California study.

Taking into account estimates currently provided by the WHO on the impact of diet on cancer risk, I estimate that such a diet / programme would reduce the overall risk of clinical cancer by perhaps 70 or even 80%. And surely the best way to win an otherwise un-winnable war is to avoid the battle altogether!

Dr Paul Clayton

Past President of the Forum on Food and Health at theRoyal Society of Medicine.

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